Piceatannol induces apoptotic cell death through activation of caspase-dependent pathway and upregulation of ROS-mediated mitochondrial dysfunction in pancreatic cancer cells

Çınar Ayan İ., Güçlü E., Vural H., Dursun H. G.

Molecular Biology Reports, vol.49, no.12, pp.11947-11957, 2022 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 49 Issue: 12
  • Publication Date: 2022
  • Doi Number: 10.1007/s11033-022-08006-8
  • Journal Name: Molecular Biology Reports
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, MEDLINE, Veterinary Science Database
  • Page Numbers: pp.11947-11957
  • Keywords: Piceatannol, Pancreatic cancer cells, Apoptosis, Anticancer agents, Phenolic compound, Resveratrol-analogue
  • Yozgat Bozok University Affiliated: No


Background: Piceatannol is a naturally occurring plant-derived phenolic compound (stilbenoid), an analogue of resveratrol. It has been shown that, piceatannol has biological activity properties such as antiproliferative, antioxidative, anti-inflammatory and proapoptotic, in various human cancer studies in vitro and in vivo. Objectives and methods: In this study, it was aimed to investigate whether piceatannol induces apoptosis through anticancer activity methods (cell viability, colony formation, annexin-V/7-AAD, ROS (Reactive oxygen species), MMP (Mitochondrial membrane potential), wound healing, invasion assay, RT-qPCR (Real-Time Quantitative Polymerase Chain Reaction), western blotting in PANC-1 and MIA PaCa-2 pancreatic cancer (PC) cell lines. Results: According to our results, piceatannol decreased cell viability in a dose and time-dependent manner [the half-maximal inhibitory concentration (IC50): 60 µM in PANC-1 and IC50: 90 µM in MIA PaCa-2 cell line at 48 h (h)] and caused significant changes in the expression of apoptosis-related genes and protein. Piceatannol induced apoptosis in PANC-1 and MIA PaCa-2 cells, accompanied by increased ROS production, decreased MMP, and increased Caspase-3-9 activity. Piceatannol also inhibited colony-forming abilities, invasion, and migration of PC cells. Conclusion: Our results show that piceatannol has an anti-cancerogenic effect on PANC-1 and MIA PaCa-2 cells, and exerts this effect by suppressing proliferation and inducing apoptosis. Therefore, piceatannol could be considered to be a potential chemotherapeutic agent candidate for the treatment and prevention of PC. Graphical abstract: [Figure not available: see fulltext.].